Molecular mechanism controlling leukocyte trafficking and its role in adaptive immune responses

2016 Fiscal Year Final Research Report

• Project Area: Analysis and synthesis of multi-dimensional immune organ network
• Project/Area Number: 24111007
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Kyushu University
• Principal Investigator: Fukui Yoshinori 九州大学, 生体防御医学研究所, 教授 (60243961)
• Co-Investigator(Kenkyū-buntansha): 戸村 道夫 大阪大谷大学, 薬学部, 教授 (30314321)
• Project Period (FY): 2012-06-28 – 2017-03-31
• Keywords: 免疫応答 / 細胞運動 / シグナル分子 / 低分子量Gタンパク質 / 蛍光プローブ / イメージング / アレルギー / 炎症

Outline of Final Research Achievements

In this study, we aimed to elucidate the mechanism controlling leukocyte trafficking during adaptive immune responses and to obtain quantitative information on immune cell migration between lymphoid tissues. We have revealed that 1) DOCK8 plays a key role in migration of dendritic cells and macrophages by linking Cdc42 activation to actomyosin dynamics through the association with LRAP35a; and 2) CD4+ T cells from DOCK8-deficient mice produce large amounts of IL-31, a major pruritogen associated with atopic dermatitis, depending on the transcriptional factor EPAS1. In addition, we developed knock-in mice expressing photoconvertible protein KikGR and quantitatively analyzed migration of various subsets of leukocytes under steady and inflammatory conditions.

Free Research Field

免疫学